title: Fish oil supplementation ameliorates fructose-induced hypertriglyceridemia and insulin resistance in adult male rhesus macaques.
abstract: Fish oil (FO) is a commonly used supplemental source of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), 2 n-3 (ω-3) polyunsaturated fatty acids (PUFAs) that have been shown to have a variety of health benefits considered to be protective against cardiometabolic diseases. Although the effects of EPA and DHA on lipid metabolism have been extensively studied, not all of the metabolic effects of FO-derived n-3 PUFAs have been characterized. Our laboratory recently showed that a high-fructose diet in rhesus monkeys induces the features of metabolic syndrome (MetS) similar to those observed in humans. Thus, we specifically wanted to evaluate the effects of FO in rhesus monkeys fed a high-fructose diet and hypothesized that FO supplementation would mitigate the development of fructose-induced insulin resistance, dyslipidemia, and other cardiometabolic risk factors. In this study, adult monkeys (aged 12-20 y) received either a standard unpurified diet plus 75 g fructose/d (control group; n = 9) or a standard unpurified diet, 75 g fructose/d, and 4 g FO (16% EPA + 11% DHA)/d (treatment group; n = 10) for 6 mo. Importantly, our results showed that daily FO supplementation in the monkeys prevented fructose-induced hypertriglyceridemia and insulin resistance as assessed by intravenous-glucose-tolerance testing (P ≤ 0.05). Moreover, FO administration in the monkeys prevented fructose-induced increases in plasma apolipoprotein (Apo)C3, ApoE, and leptin concentrations and attenuated decreases in circulating adropin concentrations (P ≤ 0.05). No differences between the control and FO-treated monkeys were observed in body weight, lean mass, fat mass, or fasting glucose, insulin, and adiponectin concentrations. In conclusion, FO administration in a nonhuman primate model of diet-induced MetS ameliorates many of the adverse changes in lipid and glucose metabolism induced by chronic fructose consumption.
authors.affiliation: Departments of Pediatrics, and.
authors.forename: Andrew A
authors.initials: AA
authors.lastname: Bremer
authors.forename: Kimber L
authors.initials: KL
authors.lastname: Stanhope
authors.forename: James L
authors.initials: JL
authors.lastname: Graham
authors.forename: Bethany P
authors.initials: BP
authors.lastname: Cummings
authors.forename: Steve B
authors.initials: SB
authors.lastname: Ampah
authors.forename: Benjamin R
authors.initials: BR
authors.lastname: Saville
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Havel
mesh_terms: D052242:Adiponectin / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004281:Docosahexaenoic Acids / Q000008:administration & dosage; D050171:Dyslipidemias / Q000097:blood; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage; D005395:Fish Oils / Q000008:administration & dosage*; D005632:Fructose / Q000009:adverse effects*; D005951:Glucose Tolerance Test; D015228:Hypertriglyceridemia / Q000097:blood / Q000139:chemically induced / Q000473:pathology*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008253:Macaca mulatta / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000139:chemically induced / Q000473:pathology
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D005395:Fish Oils; D007328:Insulin; D004281:Docosahexaenoic Acids; D005632:Fructose; D015118:Eicosapentaenoic Acid